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1.  Strigolactone Can Promote or Inhibit Shoot Branching by Triggering Rapid Depletion of the Auxin Efflux Protein PIN1 from the Plasma Membrane 
PLoS Biology  2013;11(1):e1001474.
Shoot branching is regulated by competition between branches to export the phytohormone auxin into the main stem. The phytohormone strigolactone balances shoot system growth by making auxin export harder to establish, thus modulating the auxin transport network.
Plants continuously extend their root and shoot systems through the action of meristems at their growing tips. By regulating which meristems are active, plants adjust their body plans to suit local environmental conditions. The transport network of the phytohormone auxin has been proposed to mediate this systemic growth coordination, due to its self-organising, environmentally sensitive properties. In particular, a positive feedback mechanism termed auxin transport canalization, which establishes auxin flow from active shoot meristems (auxin sources) to the roots (auxin sinks), has been proposed to mediate competition between shoot meristems and to balance shoot and root growth. Here we provide strong support for this hypothesis by demonstrating that a second hormone, strigolactone, regulates growth redistribution in the shoot by rapidly modulating auxin transport. A computational model in which strigolactone action is represented as an increase in the rate of removal of the auxin export protein, PIN1, from the plasma membrane can reproduce both the auxin transport and shoot branching phenotypes observed in various mutant combinations and strigolactone treatments, including the counterintuitive ability of strigolactones either to promote or inhibit shoot branching, depending on the auxin transport status of the plant. Consistent with this predicted mode of action, strigolactone signalling was found to trigger PIN1 depletion from the plasma membrane of xylem parenchyma cells in the stem. This effect could be detected within 10 minutes of strigolactone treatment and was independent of protein synthesis but dependent on clathrin-mediated membrane trafficking. Together these results support the hypothesis that growth across the plant shoot system is balanced by competition between shoot apices for a common auxin transport path to the root and that strigolactones regulate shoot branching by modulating this competition.
Author Summary
Plants can adapt their form to suit the environment in which they are growing. For example, genetically identical plants can develop as a single unbranched stem or as a highly ramified bush. This broad developmental potential is possible because the shoot system is produced continuously by growing tips, known as shoot meristems. Meristems produce the stem and leaves of a shoot, and at the base of each leaf, a new meristem is formed. This meristem can remain dormant as a small bud or activate to produce a branch. Thus, the shoot system is a community of shoot meristems, the combined activity and inactivity of which shape shoot form. Here we provide evidence that growth is balanced across the Arabidopsis shoot system by competition between the shoot meristems. This competition is likely mediated by the requirement of meristems to export the plant hormone auxin in order to activate bud outgrowth. In our model, auxin in the main stem, exported from active branches, can prevent auxin export by dormant buds, thus preventing their activation. Our findings show that a second hormone, strigolactone, increases the level of competition between branches by making auxin export harder to establish. Together, these hormones balance growth across the shoot system, adjusting it according to the environmental conditions in which a plant is growing.
doi:10.1371/journal.pbio.1001474
PMCID: PMC3558495  PMID: 23382651
2.  Mutation of the cytosolic ribosomal protein-encoding RPS10B gene affects shoot meristematic function in Arabidopsis 
BMC Plant Biology  2012;12:160.
Background
Plant cytosolic ribosomal proteins are encoded by small gene families. Mutants affecting these genes are often viable, but show growth and developmental defects, suggesting incomplete functional redundancy within the families. Dormancy to growth transitions, such as the activation of axillary buds in the shoot, are characterised by co-ordinated upregulation of ribosomal protein genes.
Results
A recessive mutation in RPS10B, one of three Arabidopsis genes encoding the eukaryote-specific cytoplasmic ribosomal protein S10e, was found to suppress the excessive shoot branching mutant max2-1. rps10b-1 mildly affects the formation and separation of shoot lateral organs, including the shoot axillary meristems. Axillary meristem defects are enhanced when rps10b-1 is combined with mutations in REVOLUTA, AUXIN-RESISTANT1, PINOID or another suppressor of max2-1, FAR-RED ELONGATED HYPOCOTYL3. In some of these double mutants, the maintenance of the primary shoot meristem is also affected. In contrast, mutation of ALTERED MERISTEM PROGRAMME1 suppresses the rps10b-1axillary shoot defect. Defects in both axillary shoot formation and organ separation were enhanced by combining rps10b-1 with cuc3, a mutation affecting one of three Arabidopsis NAC transcription factor genes with partially redundant roles in these processes. To assess the effect of rps10b-1 on bud activation independently from bud formation, axillary bud outgrowth on excised cauline nodes was analysed. The outgrowth rate of untreated buds was reduced only slightly by rps10b-1 in both wild-type and max2-1 backgrounds. However, rps10b-1 strongly suppressed the auxin resistant outgrowth of max2-1 buds. A developmental phenotype of rps10b-1, reduced stamen number, was complemented by the cDNA of another family member, RPS10C, under the RPS10B promoter.
Conclusions
RPS10B promotes shoot branching mainly by promoting axillary shoot development. It contributes to organ boundary formation and leaf polarity, and sustains max2-1 bud outgrowth in the presence of auxin. These processes require the auxin response machinery and precise spatial distribution of auxin. The correct dosage of protein(s) involved in auxin-mediated patterning may be RPS10B-dependent. Inability of other RPS10 gene family members to maintain fully S10e levels might cause the rps10b-1 phenotype, as we found no evidence for unique functional specialisation of either RPS10B promoter or RPS10B protein.
doi:10.1186/1471-2229-12-160
PMCID: PMC3492191  PMID: 22963533
Shoot branching suppressor; S10e; Axillary bud; Leaf polarity; Lateral organ boundary; Auxin; Strigolactone; CUC; REV
3.  Auxin, cytokinin and the control of shoot branching 
Annals of Botany  2011;107(7):1203-1212.
Background
It has been known for many decades that auxin inhibits the activation of axillary buds, and hence shoot branching, while cytokinin has the opposite effect. However, the modes of action of these two hormones in branching control is still a matter of debate, and their mechanisms of interaction are equally unresolved.
Scope
Here we review the evidence for various hypotheses that have been put forward to explain how auxin and cytokinin influence axillary bud activity. In particular we discuss the roles of auxin and cytokinin in regulating each other's synthesis, the cell cycle, meristem function and auxin transport, each of which could affect branching. These different mechanisms have implications for the main site of hormone action, ranging from systemic action throughout the plant, to local action at the node or in the bud meristem or leaves. The alternative models have specific predictions, and our increasing understanding of the molecular basis for hormone transport and signalling, cell cycle control and meristem biology is providing new tools to enable these predictions to be tested.
doi:10.1093/aob/mcr069
PMCID: PMC3091808  PMID: 21504914
Shoot branching; axillary bud; dormancy; auxin; cytokinin; canalization; polar auxin transport stream; cell cycle
4.  FTIP1 Is an Essential Regulator Required for Florigen Transport 
PLoS Biology  2012;10(4):e1001313.
FT-INTERACTING PROTEIN 1 is a novel protein that is involved in transporting florigen, a long-known mobile signal that induces flowering in plants in response to day length, from companion cells to sieve elements in the phloem of Arabidopsis.
The capacity to respond to day length, photoperiodism, is crucial for flowering plants to adapt to seasonal change. The photoperiodic control of flowering in plants is mediated by a long-distance mobile floral stimulus called florigen that moves from leaves to the shoot apex. Although the proteins encoded by FLOWERING LOCUS T (FT) in Arabidopsis and its orthologs in other plants are identified as the long-sought florigen, whether their transport is a simple diffusion process or under regulation remains elusive. Here we show that an endoplasmic reticulum (ER) membrane protein, FT-INTERACTING PROTEIN 1 (FTIP1), is an essential regulator required for FT protein transport in Arabidopsis. Loss of function of FTIP1 exhibits late flowering under long days, which is partly due to the compromised FT movement to the shoot apex. FTIP1 and FT share similar mRNA expression patterns and subcellular localization, and they interact specifically in phloem companion cells. FTIP1 is required for FT export from companion cells to sieve elements, thus affecting FT transport through the phloem to the SAM. Our results provide a mechanistic understanding of florigen transport, demonstrating that FT moves in a regulated manner and that FTIP1 mediates FT transport to induce flowering.
Author Summary
The transition to flowering is the most dramatic phase change in flowering plants and is crucial for reproductive success. Such a transition from vegetative to reproductive growth is controlled by seasonal changes in day length. Studies originally performed in the 1930s were the first to suggest that day length is perceived by a plant's leaves; by contrast, flower formation takes place in the shoot apical meristem (the tip of the shoot that gives rise to plant organs, such as leaves and flowers). The term “florigen” was later proposed to describe a mobile floral stimulus that moves from leaves to the shoot apical meristem to induce flowering. It is only recently that FLOWERING LOCUS T (FT) in Arabidopsis, and its orthologs in various other plant species, was identified as being florigen, but how florigen is transported in plants remains completely unknown. Here, we report that a novel ER membrane protein, FT-INTERACTING PROTEIN 1 (FTIP1), interacts with FT in companion cells of the phloem (a specialized type of parenchyma cell in the phloem of the plant's vascular system) and mediates FT protein movement from companion cells to sieve elements (the conducting cells of the phloem), thus affecting FT transport to the shoot apical meristem in Arabidopsis. To our knowledge, this study reveals the first regulator that is required for florigen transport and offers new insights into possible florigen transport mechanisms in other flowering plants.
doi:10.1371/journal.pbio.1001313
PMCID: PMC3328448  PMID: 22529749
5.  phot1 Inhibition of ABCB19 Primes Lateral Auxin Fluxes in the Shoot Apex Required For Phototropism 
PLoS Biology  2011;9(6):e1001076.
It is well accepted that lateral redistribution of the phytohormone auxin underlies the bending of plant organs towards light. In monocots, photoreception occurs at the shoot tip above the region of differential growth. Despite more than a century of research, it is still unresolved how light regulates auxin distribution and where this occurs in dicots. Here, we establish a system in Arabidopsis thaliana to study hypocotyl phototropism in the absence of developmental events associated with seedling photomorphogenesis. We show that auxin redistribution to the epidermal sites of action occurs at and above the hypocotyl apex, not at the elongation zone. Within this region, we identify the auxin efflux transporter ATP-BINDING CASSETTE B19 (ABCB19) as a substrate target for the photoreceptor kinase PHOTOTROPIN 1 (phot1). Heterologous expression and physiological analyses indicate that phosphorylation of ABCB19 by phot1 inhibits its efflux activity, thereby increasing auxin levels in and above the hypocotyl apex to halt vertical growth and prime lateral fluxes that are subsequently channeled to the elongation zone by PIN-FORMED 3 (PIN3). Together, these results provide new insights into the roles of ABCB19 and PIN3 in establishing phototropic curvatures and demonstrate that the proximity of light perception and differential phototropic growth is conserved in angiosperms.
Author Summary
Plants depend on sunlight for photosynthesis and adapt their growth to optimize light capture. Phototropism, the reorientation of growth towards light, is one important adaptive response. Modern studies of phototropism began with experiments in monocotyledonous grasses by Charles Darwin and led ultimately to the discovery of the plant growth hormone auxin, establishing the concept that light perception at the shoot apex triggers differential bending in the tissues below. In the past two decades, molecular-genetic analysis in the model flowering plant Arabidopsis thaliana has identified the principle photoreceptor for phototropism, phot1, as well as the major auxin transporters. Despite extensive efforts, how the photoreceptor regulates auxin transport so as to establish differential growth is still poorly understood, as is whether this process is conserved between monocots and dicots. Here, we introduce a new approach to the study of Arabidopsis phototropism in the absence of developmental events associated with seedling photomorphogenesis. In doing so, we show that the proximity of light perception and differential growth is conserved between monocots and dicots: in both plant types, differential growth is a consequence of lateral auxin movements across the shoot apex. Moreover, we identify two auxin transporters, PIN3 and ABCB19, that contribute to these movements, the latter serving to prime lateral auxin fluxes in the shoot apex. ABCB19 function is regulated by phot1, identifying it as a substrate for this class of photoreceptor kinase.
doi:10.1371/journal.pbio.1001076
PMCID: PMC3110179  PMID: 21666806
6.  Genetic Control of Organ Shape and Tissue Polarity 
PLoS Biology  2010;8(11):e1000537.
A combination of experimental analysis and mathematical modelling shows how the genetic control of tissue polarity plays a fundamental role in the development and evolution of form.
The mechanisms by which genes control organ shape are poorly understood. In principle, genes may control shape by modifying local rates and/or orientations of deformation. Distinguishing between these possibilities has been difficult because of interactions between patterns, orientations, and mechanical constraints during growth. Here we show how a combination of growth analysis, molecular genetics, and modelling can be used to dissect the factors contributing to shape. Using the Snapdragon (Antirrhinum) flower as an example, we show how shape development reflects local rates and orientations of tissue growth that vary spatially and temporally to form a dynamic growth field. This growth field is under the control of several dorsoventral genes that influence flower shape. The action of these genes can be modelled by assuming they modulate specified growth rates parallel or perpendicular to local orientations, established by a few key organisers of tissue polarity. Models in which dorsoventral genes only influence specified growth rates do not fully account for the observed growth fields and shapes. However, the data can be readily explained by a model in which dorsoventral genes also modify organisers of tissue polarity. In particular, genetic control of tissue polarity organisers at ventral petal junctions and distal boundaries allows both the shape and growth field of the flower to be accounted for in wild type and mutants. The results suggest that genetic control of tissue polarity organisers has played a key role in the development and evolution of shape.
Author Summary
Genes are known to control the shape of biological structures, like flowers, hearts, and limbs, yet how they do this is poorly understood. A working hypothesis is that genes control shape by modulating local rates at which growing tissue deforms. Evaluating this idea has been difficult, however, because of the dynamic interactions that occur within growing and deforming tissue. To address this problem, we used a combination of experimental and mathematical modelling approaches to study how genes control shape in the Snapdragon flower. This system has the advantages of having well defined genes that influence shape and being accessible to growth analysis. We first tried to explain the experimental data with a model in which genes influence local rates of tissue growth. While this model could capture many aspects of flower development, it failed to account for some key features. These could be most readily explained if genes also affect an internal field of orientations along which growth is directed, established by organisers of tissue polarity. Our analysis therefore revealed a previously unsuspected role of shape genes in the control of tissue polarity, highlighting the importance of this process for the development and evolution of tissue forms.
doi:10.1371/journal.pbio.1000537
PMCID: PMC2976718  PMID: 21085690
7.  Quantitative Control of Organ Shape by Combinatorial Gene Activity 
PLoS Biology  2010;8(11):e1000538.
A novel combination of molecular genetics, shape analysis, and computational modelling shows how the complex three-dimensional shape of the Snapdragon flower can arise through local gene activity.
The development of organs with particular shapes, like wings or flowers, depends on regional activity of transcription factors and signalling molecules. However, the mechanisms that link these molecular activities to the morphogenetic events underlying shape are poorly understood. Here we describe a combination of experimental and computational approaches that address this problem, applying them to a group of genes controlling flower shape in the Snapdragon (Antirrhinum). Four transcription factors are known to play a key role in the control of floral shape and asymmetry in Snapdragon. We use quantitative shape analysis of mutants for these factors to define principal components underlying flower shape variation. We show that each transcription factor has a specific effect on the shape and size of regions within the flower, shifting the position of the flower in shape space. These shifts are further analysed by generating double mutants and lines that express some of the genes ectopically. By integrating these observations with known gene expression patterns and interactions, we arrive at a combinatorial scheme for how regional effects on shape are genetically controlled. We evaluate our scheme by incorporating the proposed interactions into a generative model, where the developing flower is treated as a material sheet that grows according to how genes modify local polarities and growth rates. The petal shapes generated by the model show a good quantitative match with those observed experimentally for each petal in numerous genotypes, thus validating the hypothesised scheme. This article therefore shows how complex shapes can be accounted for by combinatorial effects of transcription factors on regional growth properties. This finding has implications not only for how shapes develop but also for how they may have evolved through tinkering with transcription factors and their targets.
Author Summary
A major challenge in developmental biology is to understand how patterns of gene activity are translated into complex three-dimensional forms, like hearts, wings, or flowers. Addressing this problem has not been easy, partly because of the difficulties in quantifying the effects of genes on shape and also because we lack frameworks that allow hypotheses about underlying mechanisms to be evaluated. Here we address this issue through a combination of experimental and computational approaches, using the Snapdragon flower as a model system. By quantifying the shapes of these flowers in a range of mutants with reduced or increased activity of particular genes, we show how the complex floral shape depends on the way genes act in combination in each petal region. The proposed interactions were tested by incorporating them into a computational model of the growing flower. Quantitative comparisons reveal a good agreement between the shapes generated by the model and those observed experimentally, confirming our underlying hypothesis. The Snapdragon flower, with its tightly fitting upper and lower petals, has evolved as a specialised mechanism for targeting pollinators. Our article shows how the development and evolution of such forms may have arisen by natural tinkering with the local effects of genes on growth.
doi:10.1371/journal.pbio.1000538
PMCID: PMC2976723  PMID: 21085695
8.  Alignment between PIN1 Polarity and Microtubule Orientation in the Shoot Apical Meristem Reveals a Tight Coupling between Morphogenesis and Auxin Transport 
PLoS Biology  2010;8(10):e1000516.
Imaging and computational modeling of the Arabidopsis shoot meristem epidermis suggests that biomechanical signals coordinately regulate auxin efflux carrier distribution and microtubule patterning to orchestrate the extent and directionality of growth.
Morphogenesis during multicellular development is regulated by intercellular signaling molecules as well as by the mechanical properties of individual cells. In particular, normal patterns of organogenesis in plants require coordination between growth direction and growth magnitude. How this is achieved remains unclear. Here we show that in Arabidopsis thaliana, auxin patterning and cellular growth are linked through a correlated pattern of auxin efflux carrier localization and cortical microtubule orientation. Our experiments reveal that both PIN1 localization and microtubule array orientation are likely to respond to a shared upstream regulator that appears to be biomechanical in nature. Lastly, through mathematical modeling we show that such a biophysical coupling could mediate the feedback loop between auxin and its transport that underlies plant phyllotaxis.
Author Summary
The proper development of plant organs such as leaves or flowers depends both on localized growth, which can be controlled by the plant hormone auxin, and directional growth, which is dependent on each cell's microtubule cytoskeleton. In this paper we show that at the shoot apex where organs initiate the orientation of the microtubule cytoskeleton is correlated with the orientation of the auxin transporter PIN1, suggesting coordination between growth patterning at the tissue level and directional growth at the cellular level. Recent work has indicated that mechanical signals play a role in orienting the plant microtubule network, and here we show that such signals can also orient PIN1. In addition, we demonstrate through mathematical modeling that an auxin transport system that is coordinated by mechanical signals akin to those we observed in vivo is sufficient to give rise to the patterns of organ outgrowth found in the plant Arabidopsis thaliana.
doi:10.1371/journal.pbio.1000516
PMCID: PMC2957402  PMID: 20976043
9.  Strigolactone regulation of shoot branching in chrysanthemum (Dendranthema grandiflorum) 
Journal of Experimental Botany  2010;61(11):3069-3078.
Previous studies of highly branched mutants in pea (rms1–rms5), Arabidopsis thaliana (max1–max4), petunia (dad1–dad3), and rice (d3, d10, htd1/d17, d14, d27) identified strigolactones or their derivates (SLs), as shoot branching inhibitors. This recent discovery offers the possibility of using SLs to regulate branching commercially, for example, in chrysanthemum, an important cut flower crop. To investigate this option, SL physiology and molecular biology were studied in chrysanthemum (Dendranthema grandiflorum), focusing on the CCD8/MAX4/DAD1/RMS1/D10 gene. Our results suggest that, as has been proposed for Arabidopsis, the ability of SLs to inhibit bud activity depends on the presence of a competing auxin source. The chrysanthemum SL biosynthesis gene, CCD8 was cloned, and found to be regulated in a similar, but not identical way to known CCD8s. Expression analyses revealed that DgCCD8 is predominantly expressed in roots and stems, and is up-regulated by exogenous auxin. Exogenous SL can down-regulate DgCCD8 expression, but this effect can be overridden by apical auxin application. This study provides evidence that SLs are promising candidates to alter the shoot branching habit of chrysanthemum.
doi:10.1093/jxb/erq133
PMCID: PMC2892150  PMID: 20478970
Auxin; CCD8; chrysanthemum; shoot branching; strigolactone
10.  A Rho Scaffold Integrates the Secretory System with Feedback Mechanisms in Regulation of Auxin Distribution 
PLoS Biology  2010;8(1):e1000282.
In plants, auxin distribution and tissue patterning are coordinated via a feedback loop involving the auxin-regulated cell polarity factor ICR1 and the secretory machinery.
Development in multicellular organisms depends on the ability of individual cells to coordinate their behavior by means of small signaling molecules to form correctly patterned tissues. In plants, a unique mechanism of directional transport of the signaling molecule auxin between cells connects cell polarity and tissue patterning and thus is required for many aspects of plant development. Direction of auxin flow is determined by polar subcellular localization of PIN auxin efflux transporters. Dynamic PIN polar localization results from the constitutive endocytic cycling to and from the plasma membrane, but it is not well understood how this mechanism connects to regulators of cell polarity. The Rho family small GTPases ROPs/RACs are master regulators of cell polarity, however their role in regulating polar protein trafficking and polar auxin transport has not been established. Here, by analysis of mutants and transgenic plants, we show that the ROP interactor and polarity regulator scaffold protein ICR1 is required for recruitment of PIN proteins to the polar domains at the plasma membrane. icr1 mutant embryos and plants display an a array of severe developmental aberrations that are caused by compromised differential auxin distribution. ICR1 functions at the plasma membrane where it is required for exocytosis but does not recycle together with PINs. ICR1 expression is quickly induced by auxin but is suppressed at the positions of stable auxin maxima in the hypophysis and later in the embryonic and mature root meristems. Our results imply that ICR1 is part of an auxin regulated positive feedback loop realized by a unique integration of auxin-dependent transcriptional regulation into ROP-mediated modulation of cell polarity. Thus, ICR1 forms an auxin-modulated link between cell polarity, exocytosis, and auxin transport-dependent tissue patterning.
Author Summary
The coordination of different cells during pattern formation is a fundamental process in the development of multicellular organisms. In plants, a unique mechanism of directional transport of the signaling molecule auxin between cells demonstrates the importance of cell polarity for tissue patterning. The direction of auxin flow is determined by polar subcellular localization of auxin transport proteins called PINs, which facilitate auxin efflux. At the same time, an auxin-mediated positive feedback mechanism reinforces the polar distribution of PINs. However, the molecular mechanisms that underlie polar PIN localization are not well understood. In eukaryotic cells, the Rho family of small GTPases function as central regulators of cell polarity. We show that a Rho-interacting protein from plants, called ICR1, is required for recruitment via the secretory system of PIN proteins to polar domains in the cell membrane. As a result, ICR1 is required for directional auxin transport and distribution and thereby for proper pattern formation. In addition, both the expression and subcellular localization of ICR1 are regulated by auxin, suggesting that ICR1 could function in a positive feedback loop that reinforces auxin distribution. Thus, ICR1 forms an auxin-modulated link between cell polarity, protein secretion, and auxin-dependent tissue patterning.
doi:10.1371/journal.pbio.1000282
PMCID: PMC2808208  PMID: 20098722
11.  pax1-1 partially suppresses gain-of-function mutations in Arabidopsis AXR3/IAA17 
BMC Plant Biology  2007;7:20.
Background
The plant hormone auxin exerts many of its effects on growth and development by controlling transcription of downstream genes. The Arabidopsis gene AXR3/IAA17 encodes a member of the Aux/IAA family of auxin responsive transcriptional repressors. Semi-dominant mutations in AXR3 result in an increased amplitude of auxin responses due to hyperstabilisation of the encoded protein. The aim of this study was to identify novel genes involved in auxin signal transduction by screening for second site mutations that modify the axr3-1 gain-of-function phenotype.
Results
We present the isolation of the partial suppressor of axr3-1 (pax1-1) mutant, which partially suppresses almost every aspect of the axr3-1 phenotype, and that of the weaker axr3-3 allele. axr3-1 protein turnover does not appear to be altered by pax1-1. However, expression of an AXR3::GUS reporter is reduced in a pax1-1 background, suggesting that PAX1 positively regulates AXR3 transcription. The pax1-1 mutation also affects the phenotypes conferred by stabilising mutations in other Aux/IAA proteins; however, the interactions are more complex than with axr3-1.
Conclusion
We propose that PAX1 influences auxin response via its effects on AXR3 expression and that it regulates other Aux/IAAs secondarily.
doi:10.1186/1471-2229-7-20
PMCID: PMC1855327  PMID: 17430601
12.  Root system architecture determines fitness in an Arabidopsis mutant in competition for immobile phosphate ions but not for nitrate ions. 
Plant root systems often have complex branching patterns. Models indicate that a complex architecture is only required for the acquisition of immobile resources, such as phosphate; mobile ions, notably nitrate, can be effectively taken up by very restricted root systems. We have tested this prediction using the axr4 mutation of Arabidopsis thaliana, the principal phenotypic effect of which is to reduce the number of lateral roots. Arabidopsis thaliana is not a host for mycorrhizal fungi and so acquires all its nutrients through the root system. In both a pot experiment and a field experiment conducted under natural conditions for A. thaliana, we found that only phosphate, and not nitrate, affected the fitness of the mutant relative to the isogenic wild-type line, Columbia. These results confirm model predictions and have implications both for the evolution of complex root systems and for the design of efficient root systems for crops.
doi:10.1098/rspb.2002.2120
PMCID: PMC1691122  PMID: 12396500
13.  Functional Genomics at the Arabidopsis Meeting 
Yeast (Chichester, England)  2000;17(3):235-237.
doi:10.1002/1097-0061(20000930)17:3<235::AID-YEA36>3.0.CO;2-X
PMCID: PMC2448372  PMID: 11025535

Results 1-13 (13)